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Editorial
. 2020 Dec 1;202(11):1489-1491.
doi: 10.1164/rccm.202009-3629ED.

Biological Mechanisms of COVID-19 Acute Respiratory Distress Syndrome

Michael A Matthay  1 , Aleksandra Leligdowicz  1   2 , Kathleen D Liu  1
Affiliations
Editorial

Biological Mechanisms of COVID-19 Acute Respiratory Distress Syndrome

Michael A Matthay et al. Am J Respir Crit Care Med. .
No abstract available

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Figures

Figure 1.
Figure 1.
Airway and alveolar biology during classical acute respiratory distress syndrome (ARDS) and coronavirus disease (COVID-19) ARDS. The alveolar–interstitial–capillary unit is similarly affected during classical ARDS and COVID-19 ARDS (left panel). In both types of ARDS, there is a marked upregulation of proinflammatory biomarkers, increase in capillary endothelial permeability, and an increase in inflammatory cells (neutrophils, monocytes, and macrophages) in the vascular and alveolar compartments. There are, however, notable differences in the types of upregulated biomarkers, with lower expression of IFNs and an increase in thrombotic mediators in COVID-19 relative to classical ARDS. Relative to the milder forms of COVID-19 ARDS, significant alterations in severe COVID-19 ARDS (right panel) include a higher severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral load in both the upper airways (nasal lumen) and in the circulation, a higher neutrophil count and activity (i.e., NET formation), increase in inflammatory biomarkers and thrombosis, greater monocyte (HLA-DR expression) and lymphocyte activation (CD8+ T-cell CD38 expression), and more damage to the alveolar–interstitial–capillary unit.
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References

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